Michiko Yoshii

Last Updated :2025/07/16

Affiliations, Positions
Graduate School of Biomedical and Health Sciences, Assistant Professor
E-mail
ymichikhiroshima-u.ac.jp

Basic Information

Academic Degrees

  • Ph.D., Hiroshima University
  • Master of Pharmaceutical Science, Hiroshima University

Educational Activity

  • [Bachelor Degree Program] School of Pharmaceutical Sciences : Program of Pharmaceutical Sciences : Pharmaceutical Sciences
  • [Bachelor Degree Program] School of Pharmaceutical Sciences : Program of Medicinal Sciences : Medicinal Sciences
  • [Master's Program] Graduate School of Biomedical and Health Sciences : Division of Integrated Health Sciences : Program of Medicinal Sciences
  • [Doctoral Program] Graduate School of Biomedical and Health Sciences : Division of Integrated Health Sciences : Program of Medicinal Sciences
  • [Doctoral Program] Graduate School of Biomedical and Health Sciences : Division of Biomedical Sciences : Program of Pharmaceutical Sciences

In Charge of Primary Major Programs

  • Pharmaceutical Sciences

Research Fields

  • Medicine,dentistry, and pharmacy;Pharmacy;Biological pharmacy
  • Medicine,dentistry, and pharmacy;Pharmacy;Medical pharmacy
  • Complex systems;Human life science;Eating habits

Research Keywords

  • NCX in ER membrane
  • nuclear LC3
  • nuclear proteasome
  • CCDC171
  • statin side effects
  • butyric acid
  • Injection compounding change
  • Nucleophagy, autophagy, mitophagy
  • TRPC3 calcium channel
  • ER stress

Affiliated Academic Societies

  • The Japanese Pharmacological Society
  • Japanease Society of Immunology
  • Society for Senescence-Accelerated Mouse (SAM) Research, 2015
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Educational Activity

Course in Charge

  1. 2025, Liberal Arts Education Program1, 1Term, Foundation biology for life science
  2. 2025, Undergraduate Education, Second Semester, Biostatistics
  3. 2025, Undergraduate Education, 2Term, Outline of Immunology
  4. 2025, Undergraduate Education, 2Term, Pharmaceutical Affairs Related Laws
  5. 2025, Undergraduate Education, 1Term, Clinical Pharmacology C
  6. 2025, Undergraduate Education, 3Term, Pharmacy Practice
  7. 2025, Graduate Education (Doctoral Program) , 4Term, Pharmacotherapeutic Research

Research Activities

Academic Papers

  1. A unique compound ameliorating endoplasmic reticulum stress and insulin resistance by binding to β tubulin, FASEB JOURNAL, 38(21), 20241115
    Link to Paper Search Results by DOI
  2. Effects of Simvastatin on RBL-2H3 Cell Degranulation, BIOLOGICAL & PHARMACEUTICAL BULLETIN, 46(7), 874-882, 202307
  3. Homocysteine causes neuronal leptin resistance and endoplasmic reticulum stress, PLOS ONE, 17(12), 20221213
    Link to Paper Search Results by DOI
  4. Bile acid sulfonate and 7-alkylated bile acid analogs: effect on intestinal absorption of taurocholate and cholesterol 7a-hydroxylase activity in cultured rat hepatocytes, Steroids, 65(1), 24-28, 20000101
  5. Enhancing effect of 5a-cyrinol sulfate on mucosal membrane permeability to sodium ampicillin in rats, Eur.J.Pharmacent.Biopharmacent., 49(1), 111-117, 20000101
  6. Bile acid profiles in a peroxisomal D-3-hydroxyacyl-Co A dehydratase/D-3-hydroxyacyl-Co A dehydrogenase bifunctional protein deficiency., J. Biochem. (Tokyo), 10(3), 655-658, 19970901
  7. Comparative studies of w-hydroxylation of 5b-cholestane-3a,7a,12a-triol in the mitochondrial and microsomal fraction of the liver from several vertebrates., Steroids, 62(6), 458-461, 19970601
  8. Comparison of side chain oxidation of potential C27-bile acid intermediates between mitochondria and peroxisomes of the rat liver: presence of b-oxidation activity for bile acid biosynthesis in mitochondria., J. Lipid Res., 37(12), 2550-2556, 19960401
  9. Bile salts of the toad, Bufo marinus: characterization of a new unsaturated higher bile acid, 3a,7a,12a,26-tetrahydroxy-5b-cholest-23-en-27-oic acid., J. Lipid Res., 35(9), 1646-1651, 19950901
  10. Comparative studies of metabolism of simultaneously administered chenodeoxycholic acid and ursodeoxycholic acid in hamsters., Steroids, 59(7), 431-435, 19940701
  11. Synthesis of 5b-cholestane-3a,6b,7a,25,26-pentol and identification of a novel bile alcohol, a-trichechol, present in the West Indian Nanatee bile., Chem. Pharm. Bull., 37(7), 1852-1854, 19890701
  12. Enhancing effect of 5a-cyprinol sulfate on mucosal membrane permeability to ampicillin in rats., Eur.J.Pharmac.Biopharm., 49(2), 111-117, 20000301
  13. Bile acid sulfonate and 7-alkylated bile acid analogs:Effects on the intestinal absorption of taurocholate and cholesterol 7a-hydroxylase in cultured rat hepatocytes., Steroids, 65(1), 24-28, 20000101
  14. Bile acid profiles in a peroxisomal D-3-hydroxyacyl-CoA dehydratase/D-3hydroxyacyl-CoA dehydrogenase bifunctional protein deficiency., J. Biochem., 122(3), 665-668, 19970301
  15. Comparative studies on w-hydroxylation of 5b-cholestane-3a,7a,12a-triol in the mitochondrial and microsomal fraction of the liver from several vertebrates., Steroids, 62(6), 458-461, 19970601
  16. Comparison of side chain oxidation of potential bile acid intermediates between mitochondria and peroxisomes of the rat liver: presence of b-oxidation activity for bile acid biosynthesis in mitochondria., J. Lipid Res., 37(12), 2550-2556, 19961201
  17. Comparative studies of metabolism of simultaneously administered chenodeoxycholic acid and ursodeoxycholic acid in hamsters., Steroids, 59(7), 431-435, 19940701
  18. Bile salts of the toad, Bufo marinus:characterization of a new unsaturated higher bile acid, 3a,7a,12a,26-tetrahydroxy-5b-cholest-23-en-27-oic acid., J. Lipid Res., 35(9), 1646-1651, 19940901
  19. Hypocholesterolemic effect of ursodeoxycholylcysteic acid in hamsters fed a high cholesterol diet., J. Pharmacobio-Dyn., 15(10), 573-580, 19920101
  20. Synthesis of 5b-cholestane-3a,6b,7a,25,26-pentol and identification of a novel bile alcohol, a-trichechol, present in the west indian manatee bile., Chem. Pharm. Bull., 37(7), 1852-1854, 19890701
  21. Bile alcohol profiles in bile, urine, and feces of a patient with cerebrotendinous xanthomatosis, J. Biochem., 99, 477-483, 19860401
  22. Bile acid profiles in bile, urine, and feces of a patient with cerebrotendinous xanthomatosis, Steroids, 48, 109-119, 19860401
  23. Synthesis of 5b-cholestane-3a,6b,7a,25,26-pentol and identification of novel bile alcohol, a-trichechol, present in the West Indian manatee bile, Chem. Pharm. Bull., 37, 1852-1854, 19890401
  24. Synthesis of new bile salt analogues, sodium 3a,7a-dihydroxy-5b-cholane-24-sulfonate and sodium 3a,7b-dihydroxy-5b-cholane-24-sulfonate, J. Lipid Res., 31, 1323-1326, 19900401
  25. Identification of 3,6,7,12-tetrahydroxy-5b-cholan-24-oic acids in human biologic fluids, Steroids, 55, 512-515, 19900401
  26. Metabolism of sodium 3a,7a-dihydroxy-5b-cholane-24-sulfonate in hamsters, J. Biochem., 109, 879-881, 19910401
  27. Synthesis of sulfonate analogs of bile acids, Steroids, 57, 193-198, 19920401
  28. Bile acid sulfonate alter cholesterol gallstone incidence in hamsters, Hepatology, 17, 103-110, 19930401
  29. Metabolism of sulfonate analogs of ursodeoxycholic acid and their effects on biliary bile acid composition in hamsters, J. Lipid Res., 34, 429-435, 19930401
  30. Comparative studies of metabolism of simultaneously administered chenodeoxycholic acid and ursodeoxycholic acid in hamsters, Steroids, 59, 431-435, 19940401
  31. Bile salts of the toad, Bufo marinus: characterization of a new unsaturated higher bile acid, 3a,7a,12a,26-tetrahydroxy-5b-cholest-23-en-27-oic acid, J. Lipid Res., 35, 1646-1651, 19940401
  32. Synthesis and metabolism of sodium 3a,7a-dihydroxy-25,26-bishomo-5b-cholane-26-sulfonate in the hamster, Lipids, 30, 71-78, 19950401
  33. Effect of some sulfonate analogues of ursodeoxycholic acid on biliary lipid secretion in the rat, J. Lipid Res., 37, 1181-1188, 19960401
  34. Differential inhibition of transient and long-lasting calcium channel currents by benzodiazepines in neuroblastoma cells., Brain Research, 606, 244-250, 19930401
  35. Psychotropic drugs block voltage-gated ion channels in neuroblastoma cells., Brain Research, 476, 140-144, 19890401
  36. Bile acid profiles in a peroxisomal D-3-Hydroxyacyl-CoA Dehydratase/D-3-Hydroxyacyl-CoA Dehydrogenase bifunctional protein deficiency., J. Biochem., 122, 655-658, 19970401
  37. Different changes of disuse atrophy with normally temperature and low-temperature environment on hindlimb unloadong syrian hamster., Cryoletters, 215-222, 20021201
  38. Disuse atrophy alterations in normal and low temperature environments during hindlimb unloading in syrian hamsters, Cryoletters, 24(4), 245-252, 20030701
  39. Disuse atrophy alterations in normal and low temperature environments during hindlimb unloading in syrian hamsters., Cryoletters, 24(4), 245-252, 20030701
  40. Analysis of pharmacological and molecural mechanisms underlying histamine-secretion with video-micorscopes in RBL-2H3 cells., Histamine Research in the New Millennium, 103, 20011001
  41. Caspase 3-activating Factor and Early Apoptosis Signaling in Hindlimb Unloading-induced Muscle Atrophy, European Journal of Applied Physiology, 38(3), 115-122, 20030801
  42. Diffuse atrophy alterations in normal and low temperature environments during hindlimb unloading in Syrian hamsters., Cryoletters, 24, 245-252, 20030401
  43. Endoplasmic Reticulum Stress Induces Leptin Resistanc, Molecular Pharmacology, 74(6), 1610-1619, 20080828
  44. Comparative Study of Drug Efficacy and Drug Additives between Generic Drugs and Original Drugs, 127(12), 2035-2044, 20071201
  45. Bile acid sulfonate and 7-alkylated bile acid analogs: effect on intestinal absorption of taurocholate and cholesterol 7 alpha-hydroxylase activity in cultured rat hepatocytes, STEROIDS, 65(1), 24-28, 200001
    Link to Paper Search Results by DOI
  46. Enhancing effect of 5 alpha-cyprinol sulfate on mucosal membrane permeability to sodium ampicillin in rats, EUROPEAN JOURNAL OF PHARMACEUTICS AND BIOPHARMACEUTICS, 49(2), 111-117, 200003
    Link to Paper Search Results by DOI
  47. Disuse atrophy alterations in normal and low temperature environments during hindlimb unloading in Syrian hamsters, CRYOLETTERS, 24(4), 245-252, 2003
    Link to Paper Search Results by DOI
  48. Effect of the drug containing purine skeleton on IgE/antigen-induced Histamine release, YAKUGAKU ZASSHI-JOURNAL OF THE PHARMACEUTICAL SOCIETY OF JAPAN, 125, 95-96, 2005
    Link to Paper Search Results by DOI
  49. Endoplasmic reticulum stress induced leptin resistance, YAKUGAKU ZASSHI-JOURNAL OF THE PHARMACEUTICAL SOCIETY OF JAPAN, 125, 145-146, 2005
    Link to Paper Search Results by DOI
  50. Comparative study of drug efficacy and drug additives between generic drugs and original drugs, YAKUGAKU ZASSHI-JOURNAL OF THE PHARMACEUTICAL SOCIETY OF JAPAN, 127(12), 2035-2044, 200712
    Link to Paper Search Results by DOI
  51. Endoplasmic Reticulum Stress Induces Leptin Resistance, MOLECULAR PHARMACOLOGY, 74(6), 1610-1619, 200812
    Link to Paper Search Results by DOI
  52. Leptin induced GRP78 expression through the PI3K-mTOR pathway in neuronal cells, SCIENTIFIC REPORTS, 4, 20141118
    Link to Paper Search Results by DOI
  53. Implementation and Evaluation of Genetic Testing Seminars on Lifestyle-related Disease Prevention for Pharmacy Students, YAKUGAKU ZASSHI-JOURNAL OF THE PHARMACEUTICAL SOCIETY OF JAPAN, 136(2), 337-350, 201602
  54. Implementation and Evaluation of Genetic Testing Seminars about Lifestyle-related Disease Prevention in Pharmacy Insurance -The Need for Cooperation between the Pharmacy and the University in Genetic Testing-, YAKUGAKU ZASSHI-JOURNAL OF THE PHARMACEUTICAL SOCIETY OF JAPAN, 137(12), 1517-1531, 201712
  55. Mechanisms of the action of adenine on anti-allergic effects in mast cells, IMMUNITY INFLAMMATION AND DISEASE, 6(1), 97-105, 201803
    Link to Paper Search Results by DOI
  56. echanisms of the action of adenine on anti-allergic effects in mast cells., Immun Inflamm Dis., 6(1), 97-105, 201803
    Link to Paper Search Results by DOI
  57. Implementation and Evaluation of Genetic Testing Seminars about Lifestyle-related Disease Prevention in Pharmacy Insurance-The Need for Cooperation between the Pharmacy and the University in Genetic Testing., Yakugaku Zasshi, 137(12), 1517-1531, 2017
  58. Effect of the drug containing purine skeleton on IgE/antigen-induced Histamine release, YAKUGAKU ZASSHI-JOURNAL OF THE PHARMACEUTICAL SOCIETY OF JAPAN, 125, 95-96, 2005
  59. Endoplasmic reticulum stress induced leptin resistance, YAKUGAKU ZASSHI-JOURNAL OF THE PHARMACEUTICAL SOCIETY OF JAPAN, 125, 145-146, 2005
  60. The effect of bile acid analogues on histamine release from RBL-2H3 cells, YAKUGAKU ZASSHI-JOURNAL OF THE PHARMACEUTICAL SOCIETY OF JAPAN, 127, 117-118, 2007
  61. Mechanism of endoplasmic reticulum stress-induced leptin resistance, JOURNAL OF PHARMACOLOGICAL SCIENCES, 106, 134P-134P, 2008
  62. Inhibitory effect of the drug containing purine skeleton on IgE-induced histamine release, JOURNAL OF PHARMACOLOGICAL SCIENCES, 106, 199P-199P, 2008
  63. Comparative study of drug efficacy and drug additives between generic drugs and original drugs, YAKUGAKU ZASSHI-JOURNAL OF THE PHARMACEUTICAL SOCIETY OF JAPAN, 127(12), 2035-2044, 2007
  64. Endoplasmic Reticulum Stress Induces Leptin Resistance, MOLECULAR PHARMACOLOGY, 74(6), 1610-1619, 2008
  65. The mechanisms of endoplasmic reticulum stress-induced leptin-resistance: The effect of SOCS3 and PTP1B, JOURNAL OF PHARMACOLOGICAL SCIENCES, 109, 127P-127P, 2009
  66. Leptin induced GRP78 expression through the PI3K-mTOR pathway in neuronal cells, SCIENTIFIC REPORTS, 4, 2014
  67. Implementation and Evaluation of Genetic Testing Seminars on Lifestyle-related Disease Prevention for Pharmacy Students, YAKUGAKU ZASSHI-JOURNAL OF THE PHARMACEUTICAL SOCIETY OF JAPAN, 136(2), 337-350, 2016
  68. Implementation and Evaluation of Genetic Testing Seminars about Lifestyle-related Disease Prevention in Pharmacy Insurance -The Need for Cooperation between the Pharmacy and the University in Genetic Testing-, YAKUGAKU ZASSHI-JOURNAL OF THE PHARMACEUTICAL SOCIETY OF JAPAN, 137(12), 1517-1531, 2017
  69. Mechanisms of the action of adenine on anti-allergic effects in mast cells, IMMUNITY INFLAMMATION AND DISEASE, 6(1), 97-105, 2018
  70. Mechanisms of the action of adenine on anti-allergic effects in mast cells, IMMUNITY INFLAMMATION AND DISEASE, 6(1), 97-105, 2018

Invited Lecture, Oral Presentation, Poster Presentation

  1. Dynamics of the nuclear envelope protein Coiled-coil domain containing (CCDC)171 and its possible recycling to the nucleus, M Hara, M Yoshii, Y Yanase, K Ozawa, 2024/11/16, Without Invitation, Japanese, the Pharmaceutical Society of Japan, Okayama city, [Objective] In our laboratory, we isolated and identified a protein, CCDC171, which reacts with three types of antibodies against Orai1, a component protein of the calcium release-activated calcium channel, from the nuclear fraction of rat basophilic leukemia (RBL-2H3) cells, a model cell for mast cells. The function of CCDC171 is unknown, but previous studies have reported that CCDC171 is exported from the nucleus together with proteasomes and LC3 after 30 minutes of antigen-antibody stimulation, which significantly reduces the amount of CCDC171 protein in the nuclear fraction, and that K63Ub conversion of CCDC171 is involved in this nuclear export (61st Chugoku-Shikoku Branch Meeting of the Pharmaceutical Society of Japan, etc.). Currently, we speculate that the function of CCDC171 is involved in the nuclear export of unnecessary nuclear substances generated after stimulation. In this study, we investigated the changes in the nuclear fraction CCDC171 that decreased after stimulation and the possibility that CCDC171 exported to the cytoplasm is recycled to the nuclear membrane. [Methods, Results, and Discussion] 1) Changes in CCDC171 levels due to antigen-antibody stimulation over time: RBL-2H3 cells were sensitized with DNP-specific IgE antibody (0.12 μg/mL) and stimulated with antigen (DNP-BSA 20 ng/mL) every hour for up to 10 hours, after which the cells were harvested and samples were obtained. The amount of mRNA showed a tendency to decrease after stimulation, and was significantly decreased at 3 hours (45 ± 11%, p < 0.05) and 4 hours (41 ± 5%, p < 0.05), after which it increased and then rapidly increased at 8 hours (245 ± 20%, p < 0.001), after which it decreased again. The amount of CCDC171 protein in the nuclear fraction decreased to about half at 1 hour after stimulation, and then increased after 3 hours, despite the significant decrease in the amount of mRNA at 3-4 hours after stimulation. This increase in protein amount is thought to be due to replenishment by a pathway other than de novo synthesis. Since the amino acid sequence of CCDC171 contains many dileucines, we considered the possibility of clathrin-dependent recycling. 2) Effect of the clathrin inhibitor sucrose: Sucrose acts as an osmotic stimulant in addition to inhibiting clathrin. The protein amount of nuclear fraction CCDC171 was significantly decreased (32±16%, p<0.01) 40 minutes after stimulation with 0.2M sucrose. The amount of mRNA was measured over time for 90 minutes after stimulation, but it remained unchanged. It is thought that the amount of CCDC171 released into the cytoplasm was reduced by clathrin inhibition and the amount synthesized was maintained. Based on the above, it is possible that after cell stimulation, the nuclear membrane protein CCDC171 is released outside the nucleus together with nuclear waste, proteasomes, and LC3, and is recycled to the nuclear membrane via clathrin in the cytoplasm, efficiently eliminating nuclear waste.
  2. Function of the nuclear envelope protein Coiled-coil domain containing (CCDC) 171, M Yoshii, S Uemoto, M Saeki, M Yamane, K Ozawa, The 97th Annual Meeting of the Japanease Biochemical Society, 2024/11/06, Without Invitation, Japanese, the Japanease Biochemical Society, Yokohama city, [Background] We previously identified the nuclear protein CCDC171 in rat basophilic leukemia (RBL-2H3) cells by reacting with three types of antibodies against Orai1, a component protein of the calcium release-activated calcium channel. CCDC171 is a protein present in the nuclear membrane with unknown function. In this study, we analyzed the changes in CCDC171 following antigen-antibody stimulation and 0.2M sucrose hyperosmolarity stimulation using RBL-2H3 cells, and investigated its function. [Methods and Results] 1) RBL-2H3 cells sensitized with DNP-specific IgE antibody (0.5 μg/mL) showed a significant decrease in the amount of CCDC171 in the nuclear fraction after 30 minutes of antigen-antibody stimulation. This decrease was inhibited by a ubiquitin carboxyl-terminal hydrolase isozyme L1 (UCHL1) inhibitor. A similar significant decrease in the amount of CCDC171 in the nuclear fraction was observed following hyperosmolarity stimulation. 2) Immunostaining and confocal microscopy of unstimulated or stimulated RBL-2H3 cells revealed that CCDC171 and LC3 or proteasomes coexisted near the outside of the nuclear membrane after antigen-antibody stimulation. After hyperosmotic stimulation, CCDC171 and LC3 or proteasomes coexisted, but were widely present in the cytoplasm. 3) When CCDC171 was knocked down with siRNA, antigen-antibody stimulation and hyperosmotic stimulation increased LC3 and LC3II in the cytoplasm, decreased proteasomes, and increased nuclear proteasomes. 4) Immunoprecipitation of the nuclear fraction revealed an interaction between CCDC171 and Ubiquitin (Ub), but the amount of Ub bound to CCDC171 was not affected by antigen-antibody stimulation. However, analysis of nuclear fraction CCDC171 using Blue Native Page revealed that CCDC171 was K63Ub-conjugated, and K63Ub-conjugation was slightly increased by antigen-antibody stimulation and decreased by UCH-L1 inhibitor + antigen-antibody stimulation. Increased K63Ub synthesis was also observed following hyperosmotic stimulation. 5) CCDC171 has a binding domain with clathrin, which forms endosomes, but immunostaining revealed coexistence of CCDC171 and clathrin at the nuclear membrane, and immunoprecipitation of the nuclear fraction showed no binding of CCDC171 to clathrin. [Discussion] It was suggested that CCDC171 is exported from the nucleus together with proteasomes and LC3 following antigen-antibody stimulation and hyperosmotic stimulation, and may be particularly involved in the export of proteasomes. After cells respond to stimulation, many unnecessary proteins increase in the nucleus. It is thought that Ub, which is constantly bound to CCDC171 on the nuclear membrane, is converted to K63Ub by UCHL1 after cell stimulation, and that the endocytic function of K63Ub efficiently exports it from the nucleus together with proteasomes, unnecessary proteins, and LC3.
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  3. The nuclear membrane protein Coiled-coil domain containing (CCDC) 171 functions in the nuclear proteasome and LC3 export, M Yoshii, M Saeki, S Uemoto, M Yamane, M Hara, Y Yanase, K Ozawa, The 145th Annual Meeting of the Pharmaceutical Society of Japan, 2025/03/28, Without Invitation, Japanese, The Pharmaceutical Society of Japan, Fukuoka city, Background: We previously identified a nuclear protein, CCDC171, in rat basophilic leukemia (RBL-2H3) cells that reacted with three types of antibodies against Orai1, a component protein of the calcium release-activated calcium channel. CCDC171 is a protein with unknown function that exists in the nuclear membrane. In this study, we analyzed the changes in CCDC171 caused by antigen-antibody stimulation using RBL-2H3 cells and investigated its function. Methods and Results: 1) DNP-specific IgE antibody (0.5 µg/mL)-sensitized RBL-2H3 cells showed a significant decrease in the amount of CCDC171 in the nuclear fraction after 30 minutes of antigen-antibody stimulation. This decrease was inhibited by a ubiquitin carboxyl-terminal hydrolase isozyme L1 (UCHL1) inhibitor. 2) Immunostaining and confocal microscopy of unstimulated or stimulated RBL-2H3 cells revealed that CCDC171 and LC3 or proteasomes coexisted in dots outside the nucleus after antigen-antibody stimulation. We are currently creating CCDC171-GFP and plan to conduct similar studies. 3) In RBL-2H3 cells in which CCDC171 was knocked down with siRNA, increased levels of nuclear LC3 and nuclear proteasomes were observed after antigen-antibody stimulation. 4) Interaction between CCDC171 and ubiquitin (Ub) was observed by immunoprecipitation of the nuclear fraction, but the amount of Ub bound to CCDC171 was not affected by antigen-antibody stimulation. However, when nuclear fraction CCDC171 was analyzed using Blue Native Page, CCDC171 was K63Ub-conjugated, and K63Ub-conjugation increased by antigen-antibody stimulation and decreased by UCH-L1 inhibitor + antigen-antibody stimulation, suggesting that this may be the cause of CCDC171 nuclear export. 5) CCDC171 has a binding domain with the clathrin adaptor that forms endosomes, but coexistence of CCDC171 and clathrin at the nuclear membrane was not observed by immunostaining, and binding of CCDC171 to clathrin was not observed by immunoprecipitation of the nuclear fraction. [Discussion] It was suggested that CCDC171 may be exported from the nucleus together with proteasomes and LC3 upon antigen-antibody stimulation. After cells respond to stimuli, many unnecessary proteins increase in the nucleus. It is thought that Ub, which is constantly bound to the nuclear membrane CCDC171, is converted to K63Ub by UCHL1 after antigen-antibody stimulation, and the function of K63Ub allows it to be efficiently exported from the nucleus together with proteasomes, unnecessary proteins, and LC3.
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  4. The role of the nuclear envelope-localized protein Ccdc171, whose function is unknown, in antigen-antibody stimulation, Seishiro Uemoto, Michiko Yoshii, Maya Yamane, Koichiro Ozawa, The 96th Annual Meeting of the Japanese Biochemical Society, 2023/10/31, Without Invitation, Japanese, The Japanese Biochemical Society, Fukuoka city
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  5. Function of the nuclear envelope protein Coiled-coil domain containing (CCDC) 171, Michiko Yoshii, Seishiro Uemoto, Mika Saeki, Maya Yamane, Koichiro Ozawa, The 143rd Kinki Chapter Meeting of the Japanese Pharmacological Society, 2023/06/24, Without Invitation, Japanese, The Japanese Pharmacological Society, Nagoya city
  6. Function of the nuclear envelope protein Coiled-coil domain containing (CCDC) 171, Michiko Yoshii, Seishiro Uemoto, Miko Saeki, Maya Yamane, Miyu Hara, Koichiro Ozawa, 44th Symposium on Biomembrane-Drug Interactions, 2023/10/19, Without Invitation, Japanese, The Pharmaceutical Society of Japan, Division of Physics, Fukuoka city
  7. Coiled-coil domain-containing (CCDC)171, a nuclear envelope protein with unknown function, is involved in the nuclear export pathway of unwanted nuclear proteins., Michiko Yoshii, Seishiro Uemoto, Mika Saeki, Maya Yamane, Koichiro Ozawa, The 144th Annual Meeting of the Pharmaceutical Society of Japan, 2024/03/28, Without Invitation, Japanese, The Pharmaceutical Sciety of Japan, Yokohama city
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  8. Changes in the action of butyric acid depending on the timing of administration -the effect to senescence-, Matsuo Yuki, Yoshii Michiko, Ozawa Koichiro, The 143rd Annual Meeting the Pharmaceutical Society of Japan, 2023/03/26, Without Invitation, Japanese, The Pharmaceutical Society of Japan, Sapporo city
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  9. The role of nuclear protein CCDC171 to antigen antibody stimulation, Yoshii Michiko, Yamane Maya, Saeki Mika, Baba kyoko, Hara Miyu, Uemoto Seisiro, Ozawa Koichiro, The 143rd Annual Meeting the Pharmaceutical Society of Japan, 2023/03/26, Without Invitation, Japanese, The pharmaceutical society of Japan, Sapporo city
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  10. Examination aimed at further contribution to health support for local residents by pharmacists, Miura T., Ikeda K., Hosoi T., Yoshii M., Sugiyama M., Nakano M.,Nomura H., Toyomi M., Ozawa K., The 55th JPA Congress of Pharmacy and Pharmaceutical Science, 2022/10/09, Without Invitation, Japanese, Sendai city
  11. Involvement of mitochondrial dynamics in the mechanism of side effects of atorvastatin, Maemoku H., Yoshii M., Ishida F., Ozawa K., The 140th Annual Meeting the Pharmaceutical Society of Japan, 2021/11/13, Without Invitation, Japanese, The Japanese Pharmacological Society, Nara city
  12. Possibility of anti-aging effects of atorvastatin, Yoshii M., Hayashi J., Ishida F., Ozawa K., The 141st Annual Meeting the Pharmaceutical Society of Japan, 2021/03/28, Without Invitation, Japanese, The Pharmaceutical Society of Japan, hiroshima city on line
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  13. Involvement of mitochondrial dynamics in the mechanism of side effects of atorvastatin, Yoshii M., Maemoku H., Ishida F., Saika S.,Ozawa K., The 142nd Annual Meeting the Pharmaceutical Society of Japan, 2022/03/28, Without Invitation, Japanese, The Pharmaceutical Society of Japan, Nagoya city (on line)
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  14. Lifestyles related to healthy life expectancy of local residents from the viewpoint of NDB open data, Kayo Ikeda, Toru Hosoi , Michiko Yoshii , Masanori Sugiyama , Koichiro Ozawa, 2021/03/27, Without Invitation, Japanese, web, Hiroshima city
  15. Initiatives at the "Health fair (Kampo)" as a Kampo pharmacy, Ichiro Shimasaki, Kayo Ikeda , Toru Hosoi , Tsuneyo Miura , Michiko Yoshii , Masanori Sugiyama , Junichi Otani, Shingou Nakano, Yuji Nomura , Masafumi Toyomi , Koichiro Ozawa, 2021/03/27, Without Invitation, Japanese, Web, Hiroshima city
  16. Survey of local residents' attitudes regarding the duties of pharmacists, Tsuneyo Miura, Kayo Ikeda , Toru Hosoi , Michiko Yoshii , Masanori Sugiyama , Yuji Nomura , Masafumi Toyomi , Koichiro Ozawa, 2021/03/27, Without Invitation, Japanese, Web, Hiroshima city
  17. The effects of Simvastatin and PCSK9 inhibitor on degranulation of RBL-2H3 cells by antigen-antibody reaction., Michiko Yoshii, Ai Kitazaki, and Koichiro Ozawa, 2020/02/02, Without Invitation, Japanese, Hiroshima City, 【Abstract】Hypercholesterolemia is a major problem for arteriosclerosis. Mast cells in arteriosclerosis plaque induce inflammatory reaction, increase vesicular permeability, and facilitate arterial sclerosis. In this study, we evaluated the pharmacological effect of simvastatin (SV), HMG-CoA reductase inhibitor and SBC115076 (SBC), PCSK9 inhibitor, on degranulation in RBL-2H3 cells. SV decreased significantly degranulation induced by DNP-BSA, A23187 and thapsigargin (Tg). SBC had no effect. Mevalonate or geranylgeraniol cotreatment prevented the inhibition of degranulation by SV. SV had no effect on increase of [Ca2+]in by any stimulation. Immunostaining results of RBL-2H3 cells indicated SV did not change IgE and Orai1 visually. MTT assay of RBL-2H3 cells treated with SV or SBC showed no significant change. In conclusion, SV has inhibitory effect of degranulation of RBL-2H3 cells, and probably this effect is induced by altered localization of small GTPase involved with vesicle transport not by reduced cholesterol.
  18. The degranulation mechanism of RBL-2H3 cells with a calcium ionophore A23187, Natsumi Mori, Michiko Yoshii, Naoko Yokoi, Koichiro Ozawa, 22nd annual Meeting of japanease Histamine Research Society, 2020/02/01, Without Invitation, Japanese, Japanease Histamine Research Society, Hiroshima City, 【Abstract】A23187 is one of antibiotics and used widely as a calcium ionophore. The effect of A23187 has been thought as a carrier ionophore that binds with Ca2+ and then transports Ca2+ across plasma membrane. But we found A23187 could not induce degranulation and continuous [Ca2+]in increase of RBL-2H3 cells treated with YM58483, a store operated calcium (SOC) channel inhibitor under extracellular Ca2+ existence. And low concentration of A23187 could induce Ca2+ release from ER without IP3R and RyR. 5 min stimulation of RBL-2H3 cells by 500 M A23187 could aggregate STIM1, ER membrane protein, but 15min stimulation could not. And 15min stimulation lead to increased permeability of RBL-2H3 cells. Degranulation of RBL-2H3 cells by A23187 showed byphargic alteration at about 15min. These results show the different mechanism for A23187 that works first ER membrane, maybe as an ionophore, induces SOCE, neutralizes calcium ATPase (SERCA, PMCA) in consort with Ca2+, and finally changes the permeability of plasma membrane.
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  19. The effects of Simvastatin and PCSK9 inhibitor on degranulation of RBL-2H3 cells by antigen-antibody reaction., Michiko Yoshii, Ai Kitazaki, and Koichiro Ozawa, 22nd Annual Meeting of Japanese Histamine Research Society, 2020/02/01, Without Invitation, Japanese, Japanease Histamine Research Society, Hiroshima City, 【Abstract】Hypercholesterolemia is a major problem for arteriosclerosis. Mast cells in arteriosclerosis plaque induce inflammatory reaction, increase vesicular permeability, and facilitate arterial sclerosis. Cholesterol-lowering statin has anti-inflammatory effect. In this study, we evaluated the pharmacological effect of simvastatin (SV), 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor and SBC115076 (SBC), PCSK9 inhibitor, on degranulation in RBL-2H3 cells. Simvastatin inhibited degranulation induced by dinitrophenol-bovine serum albumin (DNP-BSA), A23187, calcium ionophore, and thapsigargin (Tg), SERCA inhibitor, sequencially 20%, 15%, 15% versus control. But, SBC could not induce inhibition of any degranulation. Mevalonic acid 25mM, or geranylgeraniol 10μM coexistance with simvastatin rescue the inhibition of degranulation by simvastatin. Simvastatin (150 nM) had no effect on increase of [Ca2+]in in the Tg-stimulated cells. RBL-2H3 cells treated SV 150nM for 24 hrs were immunostained with DNP-IgE-FITC and anti Orai1 antibody. SV did not reduce FITC-IgE and Orai1. MTT assay results of RBL-2H3 cells treated with SV or SBC shows no significant difference. In conclusion, simvastatin inhibited DNP-BSA, A23187 and Tg induced degranulation. The simvastatin inhibitory effect to degranulation returns with geranylgeraniol coexistance. It is probably that SV inhibitory effect of degranulation by each stimulation induced altered locatization of small GTPase (Rab family etc.) involved with vesicle transport.
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  20. The degranulation mechanism of RBL-2H3 cells with a calcium ionophore A23187, Natsumi Mori, Michiko Yoshii, Naoko Yokoi, Koichiro Ozawa, 2020/02/01, Without Invitation, Japanese
  21. Possible involvement of homocysteine on neuronal leptin resistance in obesity, Arini Isnani Preninka, Arini Isnani Preninka, Toru Hosoi, Michiko Yoshii, Koichiro Ozawa, 2019/11/23, Without Invitation, Japanese, [Background and purpose] Leptin is an anti-obesity hormone, known to control energy expenditure and food intake. Obesity patients are in a state of “leptin resistance”, which can not transduce leptin signal appropriately. In the previous study, our group reported that endoplasmic reticulum (ER) stress, which occurs through unfolded protein accumulation, may be one of the pathophysiological mechanisms of leptin resistance in obesity. In the previous study, increased level of homocysteine was suggested to cause ER stress. However, it is unknown whether homocysteine can increase leptin resistance in neuronal cells. [Experimental procedures] We examined the effect of homocysteine and its related compounds on leptin signal and ER stress in SHSY5Y Ob-Rb neuroblastoma cells. They were analyzed by Western blotting analysis. [Results and discussion] Treatment of homocysteine in SHSY5Y Ob-Rb cells inhibited leptin-induced STAT3 phosphorylation. Therefore, it is suggested that homocysteine may cause leptin resistance. In addition, when the expression levels of ER stress response genes were investigated, homocysteine increased them, suggesting that homocysteine may induce ER stress in neuronal cells. On the other hand, other compounds related to homocysteine such as methionine and cysteine, did not inhibit leptin signal. Also, they did not cause ER stress. Overall, it is suggested that one of the underlying mechanisms of neuronal leptin resistance would be mediated through homocysteine. As the homocysteine can also inhibit methylation reaction, it is in the underway analyzing the effect of methylation reaction on leptin resistance with respect to the action of homocysteine.
  22. The effect of Trpc3 channel to endoplasmic reticulum, Michiko Yoshii, Nana Kagawa, Urara Shimizu, Koichiro Ozawa, 2019/03/23, Without Invitation, Japanese, The Pharmaceutical Society of Japan, Chiba city
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  23. The effect of Trpc3 inhibitor on cell damage of RBL-2H3 cells by Tg stimulation, Nana Kagawa, Michiko Yoshii, Koichiro Ozawa, 2018/11/10, Without Invitation, Japanese, yonago city
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  24. Can atorvastatin protect decline in cognitive function of SAMP10 mice?, Michiko Yoshii1, Nozomi Cyatani2, Momoka Iriguchi2, Juna Hayashi2, Koichiro Ozawa1, Nozomi Cyatani2, Momoka Iriguchi2, Juna Hayashi2, Koichiro Ozawa1, 2018/07/15, Without Invitation, Japanese, Shizuoka Pref, 【Abstract】Atorvastatin (Atorv) is an inhibitor of 3-hydroxy-3-methyl-glutaryl-CoA reductase and cholesterol-lowering medication. We already reported that Atorv increases typical macroautophagy marker LC3II protein expression, but autophagy is not facilitated as a consequence of the report (Kaizuka et al.,Molecular Cell,2016,64,835–849) and our results for Atorv’s effects to PC12 cells. But Atorv facilitates Tau excretion from cells, prevents Tau aggregation under stimulation of Glu 4mM, and activates mitochondria in PC12 cells. And then, we reinvestigated the effect of Atorv in senescence- accelerated (SAMP10) mice. The mice in the Atorv group (30mg/kg/day plus 0.5% CMC) increases Bdnf, Nt-3, Aquaporin 4 mRNA expression compared with control group mice.
  25. The effect of simvastatin to histamine release of RBL-2H3 cells, Michiko Yoshii, Ai Kitazaki, Yayoi Mizota, Koichiro Ozawa, 2017/10/21, Without Invitation, Japanese, Tokushima city
  26. Atorvastatin has the possibility of improvement for memory decline with age., 2017/10/21, Without Invitation, Japanese, Tokushima city
  27. Genetic testing seminars for students in the faculty of pharmaceutical sciences and pharmacists: Pharmacist future direction contribute for prevention medicine, 2016/03/28, Without Invitation, Japanese, Yokohama city
  28. The effect of simvastatin to histamine release of RBL-2H3 cells, Michiko Yoshii, Ai Kitazaki, Yayoi Mizota, Koichiro Ozawa, 2015/11/01, Without Invitation, Japanese, Kouti city
  29. The role of Trpc3 in 3T3-L1 preadipocytes proliferation, Erika Yoshimoto, Michiko YOshii, Tomoko Takahashi, Koichiro Ozawa, 2015/11/01, Without Invitation, Japanese, Kouchi city
  30. Atorvastatin promotes autophagy, and has the possibility of protection Alzheimer disease, Momoka Iriguchi, Michiko Yoshii, Nozomi Chatani, KOichiro Ozawa, 2015/11/01, Without Invitation, Japanese, Kouchi city
  31. Atorvastatin promotes macro-autophagy and then probably protects neuron., Michiko Yoshii, Nozomi Chatani, MOmoka Iriguchi, Koichiro Ozawa, The 30th SAM conference, 2015/07/04, Without Invitation, Japanese, SAM reserch conference, Gifu city, 【Abstract】Atorvastatin (Atorv) is an inhibitor of 3-hydroxy-3-methyl-glutaryl-CoA reductase and cholesterol-lowering medication. We tested Atorv induced macroautophagy in PC12 cells, and then we have been investigating the effect of Atorv in senescence-accelerated (SAMP10) mice. Atorv increased typical macroautophagy marker LC3II protein expression and secreted Tau protein by Western blot analysis. The mice in the Atorv group (30mg/kg/day plus 0.5% CMC) tend to improve turn time and total locomotive activity on the pole test after 40 weeks old. And 42 weeks old SAMP10 mice had still normal cognitive function on eight-arm radial maze test, we can’t exhibit the cognitive function yet now. But Atorv treatment brought relief age-related changes, yellowing fur, and back paws function after about 20 weeks old.
  32. The possibility of nerve protection by macroautophagy promotuion of atorvastatin, Michiko Yoshii, Nozomi Chatani, Momoka Iriguchi, Koichiro Ozawa, 2015/03/25, Without Invitation, Japanese, The pharmaceutical society of Japan, Kobe city
  33. The effect of atorvstatin on cell damage with glutamate in PC 12 cell., Nozomi Chatani, Michiko Yoshii, Koichiro Ozawa, 2014/11/08, Without Invitation, Japanese, Hiroshima city
  34. The difference of cell damage by middle chain fatty acids and long chain fatty acids in clone9 cell., Michikko Yoshii, Rumi Tasaka, Misaki Suenaga, Koichiro Ozawa, The 87th Annual Meeting of the Japanese Biochemical Society, 2014/10/18, Without Invitation, Japanese, the Japanese Biochemical Society, Kyoto
  35. The relationship between store operated channel and mature of 3T3-L1 preadipocytes., 日本肥満学会アディポサイエンス・シンポジウム, 2013/08/24, Without Invitation, Japanese
  36. Possible involvement of extracellular release of damaged mitochondria in the side effects of atorvastatin., Fuma Ishida, Michiko Yoshii, Satoko Saiga, Koichiro Ozawa, The 62nd Pharmaceutical Society of Japan, Japan Pharmaceutical Association, and Japanese Society of Hospital Pharmacists Chugoku-Shikoku Branch Academic Conference, 2023/10/28, Without Invitation, Japanese, The Pharmaceutical Society of Japan, Kouchi city

Social Activities

Organizing Academic Conferences, etc.

  1. 2023/08, 2023/08
  2. 2207/31, 2207/31
  3. 2107/18, 2107/18
  4. The 141st Annual Meeting of the PharmaceuticalSociety of Japan, 2021/03, 2021/03
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  5. 2016/06, 2016/06

History as Peer Reviews of Academic Papers

  1. 2024, Current Molecular Pharmacology, Others, 1